告达庭对大鼠肝损伤的改善作用机制研究 点击下载
| 论文标题： | 告达庭对大鼠肝损伤的改善作用机制研究 |
| 英文标题： | |
| 中文摘要： | 目的 探讨告达庭改善大鼠肝损伤的作用机制。方法将SD大鼠随机分为空白组、模型组和告达庭低、高剂量组（25、50mg/kg），每组6只。采用腹腔注射（每周3次，连续8周）二乙基亚硝胺（DEN）复制大鼠肝损伤模型。造模第5周，大鼠灌胃相应药物或0.5%羧甲基纤维素钠，连续4周。检测大鼠血清中肝功能指标[丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、总蛋白（TP）和总胆红素（TBI）]及炎症因子[白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）、IL-1β]水平，观察大鼠肝脏组织病理学形态变化，检测肝脏组织中核因子κB（NF-κB）、78kDa葡糖调节蛋白（Grp78）蛋白阳性表达水平，检测肝脏组织中内质网应激相关蛋白Grp78、C/EBP同源蛋白（CHOP）、转录激活因子6（ATF6）、肌醇需求激酶1α（IRE1α）的表达水平和蛋白激酶R样内质网激酶（PERK）磷酸化水平。结果与空白组比较，模型组大鼠血清中ALT、AST、TBI、IL-6、TNF-α、IL-1β水平和肝脏组织中NF-κB、Grp78蛋白阳性表达水平以及Grp78、CHOP、ATF6、IRE1α蛋白表达水平和PERK蛋白磷酸化水平均显著升高（P＜0.05），血清中TP水平显著降低（P＜0.05）；肝小叶结构紊乱，肝细胞肿胀，细胞间分界不明显，且伴随炎症细胞浸润。与模型组相比，告达庭各剂量组大鼠上述大部分指标显著逆转（P＜0.05）；肝小叶结构较完整清晰，细胞排列趋整齐，炎症细胞浸润也有所减少。结论告达庭对DEN所致大鼠肝损伤具有明显的改善作用，其作用机制可能与抑制内质网应激和炎症反应有关。 |
| 英文摘要： | OBJECTIVE To investigate the improvement mechanism of caudatin on liver injury of rats. METHODS SD rats were randomly divided into blank group， model group， caudatin low-dose and high-dose groups （25， 50 mg/kg）， with 6 rats in each group. Diethylnitrosamine （DEN） was injected intraperitoneally three times per week for eight weeks to establish liver injury model of rats. At 5th week of modeling， the rats received relevant medicine or 0.5% sodium carboxymethylcellulose intragastrically for 4 weeks. The levels of liver function indexes [alanine transaminase （ALT）， aspartate transaminase （AST）， total protein （TP） and total bilirubin （TBI）] and inflammatory factors [interleukin （IL-6）， tumor necrosis factor α （TNF-α）， IL-1β] in serum were detected； the histopathological morphological changes of rat liver were observed； the positive protein expressions of nuclear factor κB （NF-κB） and 78 kDa glucose regulatory protein （Grp78） in liver tissue were also determined； the expressions of endoplasmic reticulum stress-related protein Grp78， C/EBP homologous protein （CHOP）， activating transcription factor 6 （ATF6） and inositol requiring enzyme 1α （IRE1α） and the level of protein kinase R-like endoplasmic reticulum kinase robertluoyi@126.com （PERK） in liver tissue were detected. RESULTS Compared with blank group， serum levels of ALT， AST， TBI， IL-6， TNF-α and IL-1β and positive expressions of NF-κB and Grp78 in liver tissue as well as protein expressions of Grp78， CHOP， ATF6 and IRE1α， PERK protein phosphorylation level were all increased significantly in model group （P＜0.05）， while the serum level of TP was decreased significantly （P＜0.05）. The disordered structure of liver lobule， swollen liver cells， unclear intercellular boundary were observed and accompanied by inflammatory cell infiltration. Compared with model group， most of the above indexes were significantly reversed in caudatin groups （P＜0.05）； the structure of hepatic lobule was relatively complete and clear， the cells were arranged orderly， and the infiltration of inflammatory cells was also reduced. CONCLUSIONS Caudatin has a significant improvement effect against DEN-induced liver injury in rats， the mechanism of which may be associated with inhibiting endoplasmic reticulum stress and inflammatory reaction. |
| 期刊： | 2023年第34卷第05期 |
| 作者： | 常志惠；补阳；刘茜；马倩；宋捷；孙娥；韦英杰；罗毅；谭晓斌 |
| 英文作者： | CHANG Zhihui，BU Yang，LIU Qian，MA Qian，SONG Jie，SUN E，WEI Yingjie，LUO Yi，TAN Xiaobin |
| 关键字： | 内质网应激；告达庭；炎症；肝损伤；二乙基亚硝胺 |
| KEYWORDS： | endoplasmic reticulum stress； caudatin； inflammation； liver injury； diethylnitrosamine |
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